Antiphospholipid syndrome (APS) is an autoimmune disorder defined as the persistent presence
of antiphospholipid antibodies (aPL) associated with recurrent thrombotic events and/or fetal
loss. The mechanisms for fetal loss in this syndrome have not yet been clearly explained,
although several hypotheses based on experimental data have been put forward. It has been
shown that proliferation of human umbilical vein endothelial cells (HUVECs) decreased
significantly in cultures that contained sera positive for anticardiolipin antibody activity collected
from patients with recurrent fetal loss. We explored the effect of ACAs on Vascular Endothelial
Growth factor- A (VEGF-A) secretion of cultured HUVECs. VEGF appears to be the most
endothelial cell-specific and unequivocal angiogenic factor. In vitro, VEGF causes endothelial
cell proliferation and migration; in vivo, it is potently angiogenic and causes vascular
permeability. We determined the effect of ACA IgG 40μg/ml and 80μg/ml on VEGF secretion
using ELISA. The results were measured in mean ± SD and expressed in pg of VEGF/5 x 10⁴
cells. P ≤ 0.05 considered significant as compared to control. The results showed that ACA
increases VEGF-A secretion and/or may bind at VEGF-A binding sites. This finding may be
useful for finding therapies for patients with recurrent miscarriages. / Access to thesis permanently restricted to Ball State community only. / Department of Physiology and Health Science
| Identifer | oai:union.ndltd.org:BSU/oai:cardinalscholar.bsu.edu:123456789/198119 |
| Date | 03 May 2014 |
| Creators | Elawam, Noura Otman |
| Contributors | Kelly-Worden, Marie L. |
| Source Sets | Ball State University |
| Detected Language | English |
Page generated in 0.0018 seconds